We aim to show that lung elastic recoil is a function of ground substance interaction with a connective tissue network. The interstitial gel must be compressed, causing a fluid loss or flow when alveolar wall is extended. A loss of fluid which is restored osmotically on relaxation will contribute to elastic recoil. We will study the length-tension (L-T) properties of alveolar wall while changing the interstitial gel through dissolution, hydration, dehydration, temperature change, or enzymes acting upon the proteoglycans. The proteoglycan content will be measured in these same tissues by histochemistry and related to any change in the forces necessary for extension of alveolar wall. The aging lung of M. nemestrina will be examined for a naturally occurring proteoglycan change and related to changes in the length-tension properties of alveolar wall or the elastic recoil properties of whole lung. In isolated experiments the volume and swelling (osmotic) pressure of synthetic gels, lung gel, and minced lung tissue are to be studied and related to the proteoglycan content. This will demonstrate the energy involved in the tissue volume change, and show it to be an appreciable part of measured tissue forces. Finally, we will examine the pressure-volume relationships of whole lung while measuring tissue volume changes to show that in the complexity of the whole organ the same alterations in tissue volume occur and that they form a part of the resistance to filling and contribute to the elastic recoil. We expect to show that in conditions where the volume of the interstitial gel may be decreased through a change in proteoglycan content (aging, emphysema, lung lavage, transplant, reimplant, or in physiologic study) by exposure to agents that shrink, dissolve, or destroy ground substance, the lung will loss elastic recoil. This study relates the tissue properties (physiology) to tissue histochemistry, making it possible to evaluate changes with age and disease.